Evidence map›Paper›PMID 34258295›Full record

ReviewJournal of diabetes research2021

Mechanism of Ferroptosis and Its Role in Type 2 Diabetes Mellitus.

Wenxin Sha, Fei Hu, Yang Xi, Yudong Chu, Shizhong Bu

Open access · goldAbstract readReview
In one paragraph

Review in Journal of diabetes research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 3 pooled it
28.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

166 citing papers in PubMed, 3 syntheses or guidelines pooled it, 256 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Integrated OAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026
    Review
  12. Review
  13. Review
  14. Review
  15. Mechanistic Role of Disulfidptosis in Type 2 Diabetes Mellitus.Molecular nutrition & food research · 2026
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

106 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Wenxin ShaDiabetes Research Center, School of Medicine, Ningbo University, Ningbo 315211, China.ORCID https://orcid.org/0000-0001-9772-4061
Fei HuDiabetes Research Center, School of Medicine, Ningbo University, Ningbo 315211, China.ORCID https://orcid.org/0000-0002-1771-8786
Yang XiDiabetes Research Center, School of Medicine, Ningbo University, Ningbo 315211, China.ORCID https://orcid.org/0000-0001-8630-5945
Yudong ChuDiabetes Research Center, School of Medicine, Ningbo University, Ningbo 315211, China.ORCID https://orcid.org/0000-0002-1949-216X
Shizhong BuDiabetes Research Center, School of Medicine, Ningbo University, Ningbo 315211, China.ORCID https://orcid.org/0000-0001-5196-6030
Ningbo University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is a novel form of nonapoptotic regulated cell death (RCD). It features iron-dependent lipid peroxide accumulation accompanied by inadequate redox enzymes, especially glutathione peroxidase 4 (GPX4). RAS-selective lethal 3 (RSL3), erastin, and ferroptosis inducing 56 (FIN56) induce ferroptosis via different manners targeting GPX4 function. Acyl-CoA synthetase long-chain family 4 (ACSL4), lysophosphatidylcholine acyltransferase 3 (LPCAT3), and lipoxygenases (LOXs) participate in the production of lipid peroxides. Heat shock protein family B member 1 (HSPB1) and nuclear receptor coactivator 4 (NCOA4) regulate iron homeostasis preventing ferroptosis caused by the high concentration of intracellular iron. Ferroptosis is ubiquitous in our body as it exists in both physiologic and pathogenic processes. It is involved in glucose-stimulated insulin secretion (GSIS) impairment and arsenic-induced pancreatic damage in the pathogenesis of diabetes. Moreover, iron and the iron-sulfur (Fe-S) cluster influence each other, causing mitochondrial iron accumulation, more reactive oxygen species (ROS) production, endoplasmic reticulum (ER) stress, failure in biosynthesis of insulin, and ferroptosis in

Indexed as

Lipid PeroxidationApoptosis Regulatory ProteinsDiabetes ComplicationsDiabetes Mellitus, Type 2Diabetic CardiomyopathiesFerroptosisHumansIronMetabolic Networks and PathwaysMevalonic AcidMitochondrial ProteinsMyocardial IschemiaPhospholipid Hydroperoxide Glutathione PeroxidaseReactive Oxygen SpeciesApoptosis Regulatory Proteinsferroptosis suppressor protein 1, humanIronMevalonic AcidMitochondrial ProteinsPhospholipid Hydroperoxide Glutathione PeroxidaseReactive Oxygen Species

Identifiers

PMID34258295
PMCPMC8257355
OpenAlexW3177084210

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.